Bilateral Cytomegalovirus (CMV) Associated Acute Oophoritis with Cortical Necrosis.
Immunohistochemical stain for CMV highlighted massive infiltration of ovarian cortex by positively staining CMV infected cells (Fig. 11), and scattered positive cells in the lamina propria as well as serosa of the colonic mucosa of an inflamed diverticulum (Fig. 12).
Cytomegalovirus (CMV) oophoritis has been rarely reported in the literature 1-6. It usually occurs as an incidental finding in immunocompromised patients, either as part of a disseminated infection or as an isolated condition. We report here a case of bilateral CMV oophoritis in a 63-year-old woman with metastatic brain lesions undergoing whole brain radiation and steroids treatment.
Bilateral CMV oophoritis is a rare pathologic finding that is usually associated with a systemic infection. It has been suggested that previously reported isolated CMV oophoritis might represent sampling error 4. Up to date, less than 10 cases of CMV oophoritis have been reported in the literature. An underlying malignancy or immunosuppressive status 2,7 is almost always present and steroid therapy has been shown to be a strong risk factor for CMV reactivation in both groups 5,7, as it is in our current case. The patient developed acute diverticulitis and duodenal ulcer following steroids therapy for metastatic cancer. The incidental finding of bilateral oophoritis might have been part of a generalized CMV infection, although we did not have the evidence of positive blood test due to prompt death of patient from gastrointestinal bleeding shortly after the colectomy.
As demonstrated in our case and previous reports, CMV oophoritis is usually clinically silent and manifests as an unexpected finding during autopsy or surgical resection, and can be easily mistaken as metastatic neoplasm. Interestingly, despite its relatively silent clinical picture, the cortical destruction and massive involvement by CMV infected cells are profound in almost all reported cases, suggesting a possible local mechanism that aggravates CMV infection in the ovaries.
The predilection of CMV to endothelial cells is thought to be important in the pathogenesis of CMV oophoritis, while obstruction of blood flow is considered a likely mechanism in both post-menopausal and pre-menopausal women 1,5,6. Our current case demonstrated prominent changes of vascular aging in the post-menopausal ovaries, including eosinophilic deposition and thickening of vessel wall leading to narrowed lumen. On the other hand, the formation of fibrin microthrombi suggested increased procoagulant activity. Studies have shown that CMV virus particles can initiate thrombin production 8.
Observations of this case are in agreement with the previous speculation that vascular involvement may represent the main mechanism causing the rare, yet extensive CMV oophoritis, especially in post-menopausal women on top of an immunocompromised condition. However, it is still unclear whether CMV reactivation in the ovaries is only a component of a terminal event or a source of widespread CMV infection.
Contributed by Jing Yu, MD, PhD and Raja Seethala, MD